Targeting Cells Causing Split Tolerance Allows Fully Allogeneic Islet Survival With Minimal Conditioning in NOD Mixed Chimeras
Version of Record online: 13 SEP 2012
© Copyright 2012 The American Society of Transplantation and the American Society of Transplant Surgeons
American Journal of Transplantation
Volume 12, Issue 12, pages 3235–3245, December 2012
How to Cite
Al-Adra, D. P., Pawlick, R., Shapiro, A. M. J. and Anderson, C. C. (2012), Targeting Cells Causing Split Tolerance Allows Fully Allogeneic Islet Survival With Minimal Conditioning in NOD Mixed Chimeras. American Journal of Transplantation, 12: 3235–3245. doi: 10.1111/j.1600-6143.2012.04260.x
- Issue online: 30 NOV 2012
- Version of Record online: 13 SEP 2012
- Received 28 June 2012, revised 19 July 2012 and accepted for publication 06 August 2012
Figure S1: Characterization of NOD.GFPB6.g7 and B6.g7NOD.GFP radiation chimeras. (A) Diabetes incidence of NOD.wt, NOD.GFP and radiation chimeras. (B) After 5 weeks, to allow for hematopoietic cell reconstitution, peripheral blood of full chimeras was assessed by flow cytometry. Full chimerism was assessed in NOD.GFPB6.g7 and B6.g7NOD.GFP mice by gating on peripheral blood live cells and determining the expression of GFP. Lymphocytes of reconstituted B6.g7 mice were 94.0 ± 1.0% NOD.GFP in origin, and reconstituted NOD.GFP mice were 96.3 ± 0.6% B6.g7 in origin. (C) Donor lymphocyte gated T and B cell frequency in peripheral blood at 5 weeks postradiation and BMT.
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